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Blood, Vol. 94 No. 2 (July 15), 1999:
pp. 600-609
P-Selectin Expression by Endothelial Cells Is Decreased in Neonatal
Rats and Human Premature Infants
Diane E. Lorant,
Wenhua Li,
Niloufar Tabatabaei,
Michael K. Garver, and
Kurt H. Albertine
From The Nora Eccles Harrison Cardiovascular Research and Training
Institute, Department of Pediatrics, University of Utah, Salt Lake
City, UT.
Decreased adhesion of neutrophils to endothelial cells and delayed
transendothelial cell migration of neutrophils have been consistently
reported in neonatal animals and humans and contribute to their
susceptibility to infection. The delayed transmigration of neutrophils
is especially prevalent in premature neonates. To define the nature of
this defect, we used an in vivo animal model of inflammation and found
that radiolabeled leukocytes from adult rats transmigrated into the
peritoneum of other adult rats 5 times more efficiently than they did
in neonatal rats (P = .05). This indicated that defects in
neonatal neutrophils could not completely account for the delayed
transmigration. Delayed transmigration in the neonatal rats correlated
with a defect in the expression of P-selectin on the surface of their
endothelial cells. We found a similar P-selectin deficiency in
endothelial cells lining mesenteric venules and umbilical veins of
human premature infants when compared with term human infants. The
decreased P-selectin in premature infants was associated with decreased
numbers of P-selectin storage granules and decreased P-selectin
transcription. Decreased P-selectin expression on the surface of
endothelial cells in preterm infants may contribute to delayed
neutrophil transmigration and increased susceptibility to infection.
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